BACKGROUND Cranberry has been studied as a potential anticancer agent as it is capable of inducing apoptosis within cancer cells. The aim of this study was to better define the mechanism by which cranberry triggers apoptosis in HL-60 cells. METHODS The study was carried on cranberry extracts (CB). Anti-apoptotic B-cell lymphoma-2 (BCL-2) and pro-apoptotic BCL-2-associated death promoter death (BAD) proteins in cell lysates were detected through Western blotting techniques. Equivalent protein loading was confirmed through anti-α-tubulin antibody. RESULTS The results showed that treatment of HL-60 cells with CB causes a significant increase in the levels of caspase-9 and caspases-3/7 and increased mitochondrial outer membrane permeability, leading to the release of cytochrome C and Smac. These apoptotic events were associated with a significant decrease in protein kinase B (AKT) phosphorylation, which caused significant increase in BAD de-phosphorylation and promoted a sequence of events that led to intrinsic apoptosis. CONCLUSION The study findings have described a molecular framework for CB-initiated apoptosis in HL-60 cells and suggested a direction for future in vivo studies investigating the anticancer effect of cranberry.

中文翻译：

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蔓越莓提取物通过抑制AKT磷酸化增加BAD活性，从而启动HL-60细胞的固有凋亡。

背景技术蔓越莓已经被研究为潜在的抗癌剂，因为它能够诱导癌细胞内的细胞凋亡。这项研究的目的是更好地定义蔓越莓触发HL-60细胞凋亡的机制。方法进行了蔓越莓提取物（CB）的研究。通过Western印迹技术检测了细胞裂解物中的抗凋亡B细胞淋巴瘤2（BCL-2）和促凋亡BCL-2相关的死亡启动子死亡（BAD）蛋白。通过抗α-微管蛋白抗体确认了等效的蛋白质负载。结果结果表明，用CB处理HL-60细胞会导致caspase-9和caspases-3 / 7的水平显着增加，并使线粒体的外膜通透性增加，从而导致细胞色素C和Smac的释放。这些凋亡事件与蛋白激酶B（AKT）磷酸化的显着降低有关，后者导致BAD去磷酸化的显着增加并促进了一系列导致内在凋亡的事件。结论该研究结果描述了CB启动的HL-60细胞凋亡的分子框架，并为进一步研究蔓越莓的抗癌作用的体内研究提供了方向。